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Promoter H3K4 methylation reveals the dynamic reinforcement of activation-induced pathways in human CD4 T cells with differential kinetics in naïve and memory cells (RNA-Seq)

ABSTRACT: The epigenetic determinants driving the rapid responses of memory CD4 T cells to antigen are currently an area of active research. While much has been done to characterize various Th subsets and their associated genome-wide epigenetic patterns, the dynamics of histone modifications during CD4 T cell activation and the differential kinetics of these epigenetic marks between naïve and memory T cells have not been evaluated. In this study we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naïve and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation predominantly occur relatively late after activation (120 hours) and reinforce activation-induced upregulation of gene expression affecting multiple pathways important to T cell activation, differentiation, and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells. Memory CD4 have substantially more promoters marked by H3K4me3 alone, and that is influenced by promoter CpG content, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during T cell activation, providing insight into the cross-talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T cell activation and function.

ORGANISM(S): Homo sapiens

PROVIDER: GSE73213 | GEO | 2016/06/01

SECONDARY ACCESSION(S): PRJNA296380

REPOSITORIES: GEO

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Promoter H3K4 methylation dynamically reinforces activation-induced pathways in human CD4 T cells

Project description:The epigenetic determinants driving the rapid responses of memory CD4 T cells to antigen are currently an area of active research. While much has been done to characterize various Th subsets and their associated genome-wide epigenetic patterns, the dynamics of histone modifications during CD4 T cell activation and the differential kinetics of these epigenetic marks between naÃ¯ve and memory T cells have not been evaluated. In this study we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naÃ¯ve and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation predominantly occur relatively late after activation (120 hours) and reinforce activation-induced upregulation of gene expression affecting multiple pathways important to T cell activation, differentiation, and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells. Memory CD4 have substantially more promoters marked by H3K4me3 alone, and that is influenced by promoter CpG content, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during T cell activation, providing insight into the cross-talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T cell activation and function. ChIP-Seq for H3K4me2, H3K4me3, and H3K27me3 in naÃ¯ve and memory CD4 T cells at rest and at 3 time points after activation with anti-CD3/CD28.

2016-06-01 | E-GEOD-73212 | biostudies-arrayexpress

Promoter H3K4 methylation dynamically reinforces activation-induced pathways in human CD4 T cells

Project description:The epigenetic determinants driving the rapid responses of memory CD4 T cells to antigen are currently an area of active research. While much has been done to characterize various Th subsets and their associated genome-wide epigenetic patterns, the dynamics of histone modifications during CD4 T cell activation and the differential kinetics of these epigenetic marks between naïve and memory T cells have not been evaluated. In this study we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naïve and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation predominantly occur relatively late after activation (120 hours) and reinforce activation-induced upregulation of gene expression affecting multiple pathways important to T cell activation, differentiation, and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells. Memory CD4 have substantially more promoters marked by H3K4me3 alone, and that is influenced by promoter CpG content, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during T cell activation, providing insight into the cross-talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T cell activation and function.

2016-06-01 | GSE73212 | GEO

Promoter H3K4 methylation reveals the dynamic reinforcement of activation-induced pathways in human CD4 T cells with differential kinetics in naÃ¯ve and memory cells (RNA-Seq)

Project description:The epigenetic determinants driving the rapid responses of memory CD4 T cells to antigen are currently an area of active research. While much has been done to characterize various Th subsets and their associated genome-wide epigenetic patterns, the dynamics of histone modifications during CD4 T cell activation and the differential kinetics of these epigenetic marks between naÃ¯ve and memory T cells have not been evaluated. In this study we have detailed the dynamics of genome-wide promoter H3K4me2 and H3K4me3 over a time course during activation of human naÃ¯ve and memory CD4 T cells. Our results demonstrate that changes to H3K4 methylation predominantly occur relatively late after activation (120 hours) and reinforce activation-induced upregulation of gene expression affecting multiple pathways important to T cell activation, differentiation, and function. The dynamics and mapped pathways of H3K4 methylation are distinctly different in memory cells. Memory CD4 have substantially more promoters marked by H3K4me3 alone, and that is influenced by promoter CpG content, reinforcing their more differentiated state. Our study provides the first data examining genome-wide histone modification dynamics during T cell activation, providing insight into the cross-talk between H3K4 methylation and gene expression, and underscoring the impact of these marks upon key pathways integral to CD4 T cell activation and function. RNA-Seq of naÃ¯ve and memory CD4 T cells at rest and at 3 time points after activation with anti-CD3/CD28.

2016-06-01 | E-GEOD-73213 | biostudies-arrayexpress

Defining CD4 T Cell Memory by the Epigenetic Landscape of CpG DNA Methylation [Affymetrix]

Project description:Memory T cells are primed for rapid responses to antigen; however, the molecular mechanisms responsible for priming remain incompletely defined. CpG methylation in promoters is an epigenetic modification, which regulates gene transcription. Using targeted bisulfite sequencing, we examined methylation of 2100 genes (56,000 CpG) mapped by deep sequencing to T cell activation in human naïve and memory CD4 T cells. 466 CpGs (132 genes) displayed differential methylation between naïve and memory cells. 21 genes exhibited both differential methylation and gene expression before activation, linking promoter DNA methylation states to gene regulation; 6 genes encode proteins closely studied in T cells while 15 genes represent novel targets for further study. 39 genes exhibited reduced methylation in memory cells coupled with increased gene expression with activation compared to naïve cells, revealing specific genes more rapidly expressed in memory compared to naïve cells and potentially regulated by DNA methylation. These findings define a DNA methylation signature unique to memory CD4 T cells and correlated with activation-induced gene expression. transcriptome of primary human naïve and memory CD4 T cells at rest and 48 hours post-activation.

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Defining CD4 T Cell Memory by the Epigenetic Landscape of CpG DNA Methylation [RNA-Seq]

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2015-01-20 | E-GEOD-59846 | biostudies-arrayexpress

Defining CD4 T Cell Memory by the Epigenetic Landscape of CpG DNA Methylation [Bisulfite-Seq]

Project description:Memory T cells are primed for rapid responses to antigen; however, the molecular mechanisms responsible for priming remain incompletely defined. CpG methylation in promoters is an epigenetic modification, which regulates gene transcription. Using targeted bisulfite sequencing, we examined methylation of 2100 genes (56,000 CpG) mapped by deep sequencing to T cell activation in human naïve and memory CD4 T cells. 466 CpGs (132 genes) displayed differential methylation between naïve and memory cells. 21 genes exhibited both differential methylation and gene expression before activation, linking promoter DNA methylation states to gene regulation; 6 genes encode proteins closely studied in T cells while 15 genes represent novel targets for further study. 39 genes exhibited reduced methylation in memory cells coupled with increased gene expression with activation compared to naïve cells, revealing specific genes more rapidly expressed in memory compared to naïve cells and potentially regulated by DNA methylation. These findings define a DNA methylation signature unique to memory CD4 T cells and correlated with activation-induced gene expression. Targeted bisulfite sequencing of primary human naïve and memory CD4 T cells at rest and 48 hours post-activation.

2015-01-20 | E-GEOD-59858 | biostudies-arrayexpress

Defining CD4 T Cell Memory by the Epigenetic Landscape of CpG DNA Methylation [Bisulfite-Seq]

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Defining CD4 T Cell Memory by the Epigenetic Landscape of CpG DNA Methylation [Affymetrix]

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Comparative analysis of the DNA methylation landscape in CD4, CD8, and B memory lineages

Project description:There is considerable evidence that epigenetic mechanisms and DNA methylation are critical drivers of immune cell lineage differentiation and activation. However, there has been limited coordinated investigation of common pathways in distinct cell types for immunological processes such as immune activation. Further, it remains unclear if the memory cell subtypes differentiate distinctly by cell lineages. We used the Illumina EPIC array to characterize the DNA methylation similarities and differences in B cell, CD4 T, and CD8 T naïve and memory cells states. Our data describe considerable overlap in CpG dinucleotides and genes with altered DNA methylation in the process of naïve to memory activation across the three lineages, clearly suggesting that common pathways exist for immune memory generation. Further, our analyses revealed specific CpG dinucleotides and genes in CD4 T and CD8 T central to effector memory differentiation. Finally, we identified unique DNA methylation patterns in TEMRA CD8 T cells compared to other CD8 T memory cell subtypes.

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